Evidence map›Paper›PMID 30575333›Full record

ArticleMolecular genetics & genomic medicine2019

MicroRNA-186 is associated with hypoxia-inducible factor-1α expression in chronic obstructive pulmonary disease.

Li Lin, Juan Sun, Duoyi Wu, Daobo Lin, Dingwei Sun, Quanni Li, Jiannan Chen, Huan Niu, Ping He, Yipeng Ding

Open access · goldAbstract read
In one paragraph

Article in Molecular genetics & genomic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 32% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 19 citations in OpenAlex.

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  13. [Inhibiting miR-186 expression alleviates mitochondrial damage in hypoxic human umbilical vein endothelial cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Li LinDepartment of Geriatrics, the Second Affiliated Hospital of Hainan Medical University, Haikou, China.
Juan SunDepartment of General Pracitce, Hainan General Hospital, Haikou, China.
Duoyi WuDepartment of General Pracitce, Hainan General Hospital, Haikou, China.
Daobo LinDepartment of General Pracitce, Hainan General Hospital, Haikou, China.
Dingwei SunDepartment of General Pracitce, Hainan General Hospital, Haikou, China.
Quanni LiDepartment of General Pracitce, Hainan General Hospital, Haikou, China.
Jiannan ChenDepartment of General Pracitce, Hainan General Hospital, Haikou, China.
Huan NiuDepartment of General Pracitce, Hainan General Hospital, Haikou, China.
Ping HeDepartment of General Pracitce, Hainan General Hospital, Haikou, China.
Yipeng DingDepartment of General Pracitce, Hainan General Hospital, Haikou, China.ORCID 0000-0002-1635-3965
Hainan General Hospital · CNHainan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicroRNAs (miRNAs) are a family of small noncoding RNAs and are essential in the regulation of gene expression. Their impacts on gene expression have been reported in various diseases. The role of hypoxia-inducible factor 1 alpha (HIF-1α) in the development and progression of chronic obstructive pulmonary disease (COPD) has also been demonstrated. However, the role of microRNA-186 (miR-186) in relation to HIF in COPD is unknown.

methodsCell culture experiments were performed using human lung fibroblast cells (MRC-5). Cell viability was determined by MTT and flow cytometry assays. Reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot analysis were used to assess the expression levels of HIF-1α and inflammatory cytokines. Dual-luciferase reporter assays were used to reveal the correlation between miR-186 and HIF-1α.

resultsAfter miR-186 transfection, the cell lines showed reduced proliferation and increased apoptosis. After overexpression of miR-186, we found that the HIF-1α expression level was reduced in MRC-5 cells. We found that miR-186 can affect apoptosis of inflammatory fibroblasts through the regulation of HIF-1α and affect the downstream signaling pathways.

conclusionsThese data suggested that miR-186 contributes to the pathogenesis of COPD and that miRNA-186 may also affect the HIF-1α-dependent lung structure maintenance program.

Indexed as

ApoptosisCell Line, TumorCell ProliferationCytokinesFibroblastsHumansHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsPulmonary Disease, Chronic ObstructiveCytokinesHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsMIRN186 microRNA, humanchronic obstructive pulmonary diseaseHIF-1αinflammatory cytokinesmiR-186

Identifiers

PMID30575333
PMCPMC6418446
OpenAlexW2906042262

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.